MicrobiologyBytes: Virology: HGV Updated: October 19, 2004 Search

Hepatitis G Virus (HGV)

History:

  • In 1967, Deinhard et al. inoculated tamarin monkeys with serum from GB, a surgeon suffering from acute hepatitis. The monkeys also showed biochemical and histologic evidence of acute viral hepatitis. Both GB and the tamarins recovered from their hepatitis: this form of the disease is self-limiting.
  • 1970s-early 80s: multiple passages in tamarins and marmosets using the serum from the tamarins originally infected with GB serum were performed. The "GB agent" was characterized biophysically (filtration, etc) and shown to be of viral origin.
  • Almeida et al (Nature, 261: 608-609, 1976) perform the 11th passage study of the "GB agent". This material was deposited at the ATCC in the USA (also known as: "H205 GB pass 11").
  • Researchers at Abbott Laboratories used GB passage 11 serum for tamarin inoculations. Serum from tamarins with hepatitis were used for molecular biology experiments designed to identify the viral "GB agent". Methods used included representational difference analysis (RDA) and cDNA library immunoscreening.
  • RDA identified cDNA fragments isolated from infectious tamarin serum with sequence similarity to other flaviviruses, but most similar to HCV. The genomes of two viruses were eventually cloned and sequenced in their entirety from the infectious tamarin serum produced at Abbott Laboratories. These viruses were designated GB viruses A and B (GBV-A, GBV-B) (Simons et al, PNAS, 92:3401-3405, 1995).
  • Serologic studies identified humans with antibodies against nonstructral proteins from GBV-A and B, but PCR studies failed to identify humans infected with GBV-A or B even though they were antibody positive.
  • Consensus (i.e. degenerate) PCR primers were designed based upon alignments of nucleotide sequences from the helicase genes of GBV-A, GBV-B, and HCV.
  • These primers identified a PCR positive individual from West Africa. The sequence of the PCR product was similar to but distinct from GBV-A and GBV-B and believed to be a portion of the genome of a third virus, designated GB virus C. (Simons et al Nature Medicine, 1: 564-569, 1995).
  • The complete genome sequence of GBV-C was determined (Leary et al, J.Med.Virol, 48: 60-67, 1996).
  • Linnen et al (Science, 271: 505-508, 1996) described the isolation of a new virus, designated HGV, from a patient diagnosed with non-ABC hepatitis.
  • Both GBV-C and HGV are positive, single-stranded RNA viruses containing approximately 9400 nucleotides, have a genomic organization resembling that of the Flaviviridae, and are distantly related to HCV. They have 86 percent nucleotide sequence similarity and 96 percent predicted amino acid sequence similarity. Thus they are considered to be different isolates of the same virus, which is now generally known as HGV.

 

HGV infection was originally suggested to be connected with fulminant hepatitis, but recent studies have failed to prove a connection between HGV and clinical illness. Some studies have suggested that in contrast to HCV, the liver is not the primary replication site for HGV (e.g. Tucker T.J. et al (2000) Evidence that the GBV-C/hepatitis G virus is primarily a lymphotropic virus. J.Med.Virol. 61: 52-8). Where does HGV grow? Virus circulating in the bloodstream is difficult precipitate with antibody to immunoglobulins, but can precipitated with antibody to apolipoproteins. Since no hypervariable regions have yet been identified in the envelope proteins of HGV, the lipoprotein coat may help the virus evade immune surveillance and contribute to its persistence.

In many countries, 1-2% of blood donors test positive for HGV RNA & the prevalence of HGV infection is up to 10-15% in West African children. How this high prevalence is maintained is unknown, but this does suggest that sub-clinical infection is common. Antibodies to E2, an envelope protein of HGV, can be detected in >50% IVDAs who are HGV RNA negative, but in relatively few IVDAs who have HGV RNA. Therefore, HGV infection is probably much more frequent than studies of the prevalence of HGV RNA suggest.

The virus is transmitted by the same routes as HCV & co-infection is common; however, this may represent a common source of infection rather than any clinical similarity between the two viruses. The clinical significance of HGV infection and HGV-HCV co-infection remains to be fully elucidated, but at present does not seem to be a major disease-causing factor. The majority of patients infected with HGV by blood transfusion do not develop chronic hepatitis, but viremia frequently persists without biochemical evidence of hepatitis. Given the high prevalence of HGV worldwide and the association with mild or no clinical illness, is HGV merely an accidental tourist that occasionally travels with other hepatitis viruses?

Viruses are obligate intracellular parasites.

But does parasite = pathogen ?

Not necessarily.

Some viruses are commensal in nature - for example, HGV and TTV - the accidental tourists.

 

Bestsellers - Music - DVDs - Videos - Electronics
Search for ... (keywords):
Search for ... (keywords):

Bestsellers - Music - DVDs - Videos - Electronics


HAV | HBV | HCV | HDV | HEV | TTV


© MicrobiologyBytes 2004.